Central serous chorioretinopathy secondary to solar retinopathy: an unusual presentation

Abstract

Solar retinopathy (SR) results from unprotected solar eclipse viewing and also from gazing at the sun for a long duration. It has been known for a long that direct viewing of the sun causes visual disruption. Usually, there is a disruption of the inner segment–outer segment junction, but an association of central serous chorioretinopathy (CSCR) with SR is quite rare. We report a case of CSCR associated with solar eclipse viewing.

Background

Solar retinopathy (SR) was first described by Bonetus during the 17th century. It is due to the thermal effects of the visible and near-infrared rays focused on the retina that damage the outer layer of the retina. SR occurs primarily through a photo-oxidative pathway rather than by direct thermal injury.¹ Phototoxicity, mainly from the high-energy Ultravoilet -A (UV-A) and the shorter wavelengths of visible light, leads to generation of reactive oxygen species and subsequent oxidative damage to these epithelial cells and the surrounding photoreceptors.^2–4 Other than viewing the unprotected solar eclipse, it can be seen in the patient with schizophrenia, sunbathers, religious rituals of sun gazing, under influence of psychedelic drugs.⁵ Although traditionally optical coherence tomography (OCT) was used for diagnosing SR, recently the use of a new setting of red, green and blue channels could improve the diagnosis and monitoring of SR, hence improving patient care.⁶ Multimodal imaging shows significant differences in the type of patient affected as well as in the signs in SR and the maculopathy produced by a laser pointer.⁷ Fundus autofluorescence (FAF) is a novel imaging technique to detect subtle solar-induced injuries of the retina.⁸ When compared with OCT and short waveFAF, near-infrared FAF is superior in detecting subtle changes.⁹ Central serous chorioretinopathy (CSCR) per se is a relatively common retinal disease characterised by the neurosensory detachment (NSD) with or without Retinal pigment epithelium (RPE) detachment of retina at the posterior pole due to accumulation of fluid. Young and middle-aged men with no previous significant medical history and no systemic symptoms or signs are commonly affected in CSCR. However, it can be associated with increased levels of endogenous or exogenous glucocorticoids.

Guyer et al concluded that hyperpermeability was at the level of the choroid rather than the RPE, which caused serous detachments of the RPE, and thus inducing a rip or decompensation of the RPE leading to neurosensory retinal detachment.¹⁰ Choroidal ischaemia causing disturbance in choroidal circulation can be a cause as noted by Hayashi et al.¹¹ Prunte and Flammer suggested a localised lobular inflammatory or ischaemic choroiditis as the cause of choroidal hyperpermeability in the area of the damaged RPE.¹² An alternative theory suggests that CSCR can result from dysfunction of RPE following an undefined insult resulting in impairment of RPE cells causing a reversal in fluid movement. This, in turn, leads to accumulation of fluid in the subretinal space, causing a neurosensory retinal detachment.¹³ So the pathomechanism of CSCR is still a matter of debate. Its association with SR is quite rare. Although the normal eye can tolerate brief glances at the sun, it requires exposure of at least 30 s to produce burns. Herein we present a case of CSCR associated with SR.

Case presentation

A 35-year-old man came to out patient department (OPD) with the blurring of vision. Visual acuity in right eye (RE) was 20/40 and in left eye (LE) was 20/32. In RE vision improved to 20/32 with +0.50 DS. On examination, the anterior segment was normal. Fundus examination of RE showed altered foveal reflex and LE fundus showed a yellowish spot at the macula. OCT was performed, which showed NSD in RE suggestive of CSCR and inner segment-outer segment junction (IS-OS junction) disruption in LE. On further inquiring patient gave the history of viewing the solar eclipse on 26^th December 2019 in Jodhpur(a district in western Rajasthan) for duration of approximately 30 s and came to eye OPD 2 weeks after the exposure. There was no history of similar episodes in the past, there were no risk factors associated with CSCR. So it was concluded that it was a case of SR in which IS-OS disruption has led to CSCR in RE. Amsler grid was performed the next day (as the patient was dilated), which showed metamorphopsia as seen by irregular lines. (figure 1)

Figure 1.

(A) Right eye optical coherence tomography (OCT) of a patient showing neurosensory detachment at presentation (2 weeks after exposure). (B) Left eye OCT of the same patient showing inner segment–outer segment disruption (ellipsoid zone) with intact external limiting membrane and retinal pigment epithelium 2 weeks after exposure.

At 1 month, NSD decreased in RE but visual acuity remained the same in both eye (BE).

At 6-month follow-up, NSD disappeared, but a hyperreflective zone was seen to involve foveola in BE on OCT suggestive of lipofuscin accumulation following degeneration of photoreceptors and RPE. Visual acuity in RE improved to 20/32 and in LE remained the same. Small central scotoma was seen on the Amsler grid in BE. (figure 2).

Figure 2.

(A) Right eye optical coherence tomography (OCT) of the patient at 6 months showing hyperreflectivity involving all layers in foveolar region suggestive of lipofuscin accumulation along with intact regenerated retinal pigment epithelium (RPE). (B) Left eye OCT of the same patient at 6 months showing hyperreflectivity involving all layers in foveolar region suggestive of lipofuscin accumulation along with intact regenerated RPE.

Investigations

OCT—It is a non-invasive technique to detect foveal impairment and location and extension of retinal injury from SR, it can even detect subtle foveal damage. The majority of patients shows IS-OS disruption with outer retinal cyst formation, NSD can be visualised and on healing hyperreflective spot in the outer retinal layer can be seen in some patients.¹⁴

Differential diagnosis

OCT finding of SR may mimic whiplash injury, ocular trauma, early macular hole, idiopathic parafoveal telangiectasia.

Treatment

Tab antioxidant was given once a day to ameliorate retinal damage.

Outcome and follow-up

Although the loss of vision attributed to SR is reversible to some extent, it can have some deleterious effects on the quality of vision that are not reversible. It requires a long-term follow-up in these patients to see whether there is some improvement or not. We followed the patient at 1 month and then at 6 months, but there was no significant change in visual acuity from baseline.

Discussion

SR is photic retinopathy occurring after direct exposure to sunlight. UV radiation is responsible for photochemical damage by various mechanisms such as free radical generation and oxygen-dependent toxicity. It is typically associated with unprotected solar eclipse viewing. Presentation commonly occurs within a few hours of exposure with impairment of the central vision, metamorphopsia, central or paracentral scotoma. Quantitative visual acuity can be variable depending on the severity of the damage.¹⁵

SR is usually bilateral as in our case, though it may have a unilateral, asymmetrical presentation. Fundus examinations in acute phases can show a small yellow spot at the fovea, encircled by faint grey granular pigmentation. This yellowish discolouration will usually become faint with time, leaving a pathognomonic reddish spot.¹⁶

Sometimes changes can be subtle to be seen only on OCT. Commonly seen signs include IS-OS disruption, outer retinal cyst formation. OCT features of the outer retina, as seen in our patient, are very crucial for the diagnostic suspicion as clinical findings are generally subtle and may be easily missed.¹⁷

CSCR results from the accumulation of subretinal fluid, NSD and leakage with angiographic evidence of RPE hyperpermeability.¹⁸ Various systemic risk factors are associated with CSCR including psychological stress, type A personality, pregnancy, untreated hypertension, corticosteroids and psychopharmacologic medications,¹⁹ but our patient had none of these factors. In fact, IS-OS disruption in other eye pointed out that CSCR resulted from the disruption caused by SR.

It might be possible that intense sunlight was preferentially absorbed by melanosomes in the RPE, causing localised RPE damage and thus causing CSCR.²⁰

In acute CSCR normally as the underlying cause is treated, choroidal hyperpermeability decreases and it leads to resolution of subretinal fluid. In chronic cases; however, RPE may transform into lipofuscin laden cells ultimately leading to atrophy.

In SR in acute cases, there is disruption to RPE, which in turn leads to dysfunction of outer photoreceptor layer. In chronic cases, RPE regenerates but as photoreceptors are in postmitotic phase, they are not regenerated and abnormal pigments such as lipofuscin may be deposited leading to hyperreflectivity on OCT or there can be atrophic changes in the retina.¹⁷

The association of CSCR with SR is very rare. To the best of our knowledge, only two cases are reported that also one developed CSCR when corticosteroids were given for the treatment of SR.^{21 22}

The treatment of SR is controversial. Most cases of SR improve over time without treatment.¹⁵ Corticosteroids might prove beneficial in the treatment of SR because of their ability to suppress inflammatory tissue reactions resulting from injury but not yet proven. But in our case, associated CSCR might get worsen due to steroids. Antioxidants and free radical scavenger ginkgo glycosides may be used to ameliorate retinal damage. So treatment is mainly conservative along with proper public awareness and education

The visual prognosis of SR is usually favourable, probably due to the resistance of foveal cones to photochemical damage, and in most cases, the visual loss is at least partly reversible.¹⁵

As it is an easily avoidable condition, prevention is of utmost importance. Therefore, awareness and sensitisation of people to this condition are required.

Limitations

1. The diagnosis was solely based on OCT and history. FAF and fundus fluorescein angiography were not performed.

2. As patient came after 2 weeks, early findings were missed.

Learning points.

• Awareness is the utmost important thing to protect our eyes from solar retinopathy.

• As solar eclipse usually attracts young, curious minds, youngsters are to be educated.

• Use of protective measures/sunglasses while viewing a solar eclipse.

• Never forget to examine the other eye as in our case we got a clue only from other eye examination.